Reversible hepatotoxicity associated with hepatic vitamin A accumulation in a protein-deficient patient.
A 62-yr-old white male presented with edema, protein malnutrition, and abnormal liver function. He had ingested from 40,000-50,000 IU of vitamin A per day for 7 yr. Examination of liver tissue by light and electron microscopy revealed findings characteristic of an excessive accumulation of vitamin A. Liver tissue contained massive amounts of vitamin A (19,000 IU/g); however, both the serum concentration of vitamin A and retinol-binding protein were below normal, and serum RBP was not saturated. On a normal diet the patient was able to mobilize hepatic vitamin A, as indicated 71 days later by a repeat biopsy of the liver, which then contained 9000 IU of vitamin A/g. During this time his nutrition improved, serum vitamin A rose, and serum RBP became transiently saturated. The amount of vitamin A ingested by this patient was less than that usually producing recognizable hepatotoxicity, and he had no extra hepatic manifestations of vitamin toxicity, consistent with a low serum vitamin A concentration and a low vitamin A to retinol-binding protein ratio. At presentation he was apparently unable to normally mobilize vitamin A from his liver, which may have been due to an accompanying protein deficiency.[1]References
- Reversible hepatotoxicity associated with hepatic vitamin A accumulation in a protein-deficient patient. Weber, F.L., Mitchell, G.E., Powell, D.E., Reiser, B.J., Banwell, J.G. Gastroenterology (1982) [Pubmed]
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